INTRODUCTION — Gynecomastia, a benign proliferation of the glandular tissue of the male breast, is common in infancy, adolescence, and in middle-aged to older men. Pseudogynecomastia, which is often seen in obese men, refers to fat deposition without glandular proliferation. Gynecomastia must be differentiated from breast carcinoma, which is far less common.
The epidemiology and pathogenesis will be reviewed here. The causes, evaluation, and management are discussed separately. (See "Clinical features, diagnosis, and evaluation of gynecomastia in adults" and "Management of gynecomastia".)
DEFINITIONS — Gynecomastia is defined histologically as a benign proliferation of the glandular tissue of the male breast and clinically by the presence of a rubbery or firm mass extending concentrically from the nipple(s) (figure 1) [1]. Fat deposition without glandular proliferation is termed pseudogynecomastia (lipomastia) and is often seen in obese men.
The most important differentiation is between gynecomastia and breast carcinoma. Carcinoma is much less common, generally unilateral, eccentric in location rather than symmetrical to the nipple, nontender, hard or firm, often fixed to the underlying tissue, and may be associated with skin dimpling, nipple retraction or discharge, and axillary lymphadenopathy [2,3]. Less common conditions leading to breast enlargement include neurofibromas, lymphangiomas, hematomas, lipomas, and dermoid cysts. (See "Clinical features, diagnosis, and evaluation of gynecomastia in adults", section on 'Further evaluation to rule out breast cancer'.)
EPIDEMIOLOGY — Gynecomastia is common in infancy, puberty, and in middle-aged to older men. One estimate is that between 60 to 90 percent of infants have transient gynecomastia due to the high estrogenic milieu of pregnancy [4]. Male infants also have a "mini-puberty" with adult serum concentrations of gonadotropins and a transient rise of serum estradiol more than serum testosterone concentrations [3]. After delivery, gynecomastia regresses in two to three weeks.
The second peak is during puberty, with a prevalence ranging from 4 to 69 percent, with a median from several studies of 33 percent (figure 2) [5-12]. This wide variation is probably due to differences in what is considered normal subareolar glandular tissue, observer differences, and, probably most importantly, differences in the age distribution of the adolescents examined. Pubertal gynecomastia usually has an onset between ages 10 and 12 years and peaks between ages 13 and 14 years, usually at Tanner pubertal stage 3 (table 1). It generally regresses within 18 months but may persist into adulthood in approximately 20 percent of affected individuals [6].
The third peak of gynecomastia occurs in middle-aged and older men. The highest prevalence is at 50 to 80 years, with as many as 24 to 65 percent of men being affected (figure 2) [13-18].
Although gynecomastia is usually bilateral, it is often asymmetrical and can even be unilateral [19,20]. In a study of 36 male patients who underwent subcutaneous mastectomy for a unilateral breast mass, 30 (83 percent) had gynecomastia, four (11 percent) had lipoma, and two had breast cancer [20]. The majority of patients with gynecomastia were receiving medications that have been associated with gynecomastia.
In adult patients with persistent gynecomastia seeking consultation for the condition, current estimates suggest the following etiologies, all of which are discussed in detail below (table 2) (see 'Causes of gynecomastia' below):
●Persistent pubertal gynecomastia – 25 percent
●Drugs – 10 to 25 percent (table 3)
●No detectable abnormality – 25 percent
●Cirrhosis or malnutrition – 8 percent
●Hypogonadism – Primary (8 percent), secondary (2 percent)
●Testicular tumors – 3 percent
●Hyperthyroidism – 1.5 percent
●Chronic kidney disease – 1 percent
A series of 786 men with gynecomastia seen at a single institution has confirmed these prevalent etiologies [21].
PATHOPHYSIOLOGY — The common mechanisms of gynecomastia include an increase in estrogen production (eg, due to increased availability of estrogen precursors for peripheral conversion to estrogen) or decreased androgen production (eg, due to hypogonadism). Androgen receptor blockade and, in men with impaired testosterone production, decreased free testosterone due to increased binding of androgen to sex hormone-binding globulin (SHBG) are other mechanisms.
There does not appear to be any difference in the responsiveness of the male or female breast glandular tissue to hormonal stimulation, but preliminary data in transwomen treated with estrogen (without a progestin) suggests that breasts of transwomen tend to remain smaller and less developed than adult cis-female breasts [22]. It is not known whether the addition of a progestin results in larger, more developed breasts in transwomen. The amount of glandular proliferation and ductal differentiation depends upon an individual's breast tissue sensitivity, the hormonal milieu, and the duration and intensity of hormonal stimulation.
Estrogens induce ductal epithelial hyperplasia, ductal elongation and branching, proliferation of the periductal fibroblasts, and an increase in vascularity. The histologic picture is similar in male and female breast tissue after exposure to estrogen. In comparison, luteal phase progesterone in women leads to acinar development that is not seen in males [23]. However, little is known about the effects of progestins on histology of adult transwoman or adult cis-men [24].
The various conditions associated with gynecomastia are usually thought to represent an imbalance between the stimulatory effect of estrogen and the inhibitory effect of androgen (figure 3) [25,26]. The factors that define the net estrogen/androgen balance are (table 4):
●The production of these steroids or their precursors by the three steroid-producing tissues (the adrenals, the testes, and the placenta)
●The extraglandular conversion of androgens to estrogens, such as in adipose tissue
●The circulating concentration and steroid hormone binding of SHBG
●The hormone target cells' ability to respond to androgens and estrogens
In utero — During pregnancy, the placenta transforms dehydroepiandrosterone and dehydroepiandrosterone sulfate (derived from both the mother and fetus) to estrone (E1) and estradiol (E2), which enter the fetal circulation and stimulate breast glandular proliferation, resulting in transient neonatal gynecomastia. (See "Placental development and physiology", section on 'Steroid hormones'.)
In adolescents and adult men — In boys who develop gynecomastia during early puberty, a relative increase in extratesticular production of estrogen plays a role in the development of gynecomastia. The major androgen secreted by the adrenal glands is androstenedione. Most of the circulating E2 and E1 in early male puberty are derived from the extraglandular conversion of testosterone and androstenedione to E2 and E1, respectively, by tissues including liver, skin, fat, muscle, bone, and kidney, all of which contain an aromatase enzyme. In mid to late pubertal adolescent boys and adult men, a relative increase in testicular production of estrogen compared with testosterone is the major cause of gynecomastia; after early puberty in males, 95 percent of the circulating testosterone, 15 percent of the E2, and less than 5 percent of E1 is directly secreted by the testes (figure 3) [5,23,27,28]. (See "Male reproductive physiology", section on 'Testosterone synthesis'.)
Sex hormone-binding globulin — The majority of androgens and estrogens that enter the circulation are relatively tightly bound to SHBG and are weakly bound to albumin. Conditions that increase SHBG concentrations (estrogenic and many antiseizure medications, aging) will decrease free testosterone in men with impaired testosterone production. In addition, SHBG has a higher affinity for androgens than for estrogens, and therefore, any substance that displaces sex hormones from SHBG will tend to displace quantitatively more estrogens than androgens. The unbound or weakly bound androgens and estrogens enter the target cells and lead to hormone action [29,30]. (See "Male reproductive physiology", section on 'Transport of gonadal steroids'.)
Imbalance between estrogen and androgen — An imbalance between estrogen and androgen action will occur if there is an absolute increase in free estrogens, a decrease in endogenous production of free androgens, an increase in the free estrogen-to-free androgen ratio, androgen insensitivity, or an estrogenic effect of drugs (figure 3). Some patients with gynecomastia, for example, have enhanced sensitivity of the breast tissue to normal circulating estrogen levels even in the presence of normal circulating androgen concentrations. This may reflect increased aromatization of androgens to estrogens in the breast tissue itself as increased aromatase activity has been found in pubic skin fibroblasts of patients with pubertal gynecomastia [31].
Obesity — In some, but not all, studies, body mass index (BMI) is positively correlated with both breast diameter and the presence of gynecomastia in both adolescents and adults [16,32]. Breast adipose tissue contains the aromatase enzyme complex that converts testosterone and androstenedione to E2 and E1, respectively. Thus, it has been hypothesized, but not proven, that an increase in breast adipose tissue due to generalized weight gain might increase local estrogen production, which in turn may stimulate breast glandular tissue proliferation in a paracrine fashion. In addition, the increase in breast fat with weight gain may lead to pseudogynecomastia, which may or may not be associated with true gynecomastia. (See "Causes of secondary hypogonadism in males", section on 'Obesity'.)
CAUSES OF GYNECOMASTIA
Physiologic
Trimodal distribution — As noted above, physiologic gynecomastia is common and has a trimodal distribution occurring in neonatal, pubertal, and older males [1,16]. (See 'In utero' above and 'In adolescents and adult men' above.)
Pubertal gynecomastia — It is likely that a transient imbalance of estrogen to androgen accounts for much of the estrogen/androgen imbalance that leads to pubertal gynecomastia. Most studies in pubertal boys with gynecomastia have found no differences in single-point measurements of serum concentrations of testosterone, estradiol (E2), estrone (E1), or gonadotropins from those in normal boys [7,9,33,34]. However, during early puberty, the serum E2 concentrations rise to adult levels before the testosterone concentration, and some reports have shown a transient increase in E2 concentration at the onset of puberty in boys who develop gynecomastia [7]. These boys may also have wider fluctuations of E2 levels, with an absolute increase in 24-hour concentration of E2, which may reflect increased conversion of adrenal androgens to estrogens [10,35].
Leptin and insulin-like growth factor-1 (IGF-1) are elevated in boys with pubertal gynecomastia compared with those without [36-39]. The finding that pubertal gynecomastia occurs in a temporal association with peak height velocity (the time when IGF-1 levels also peak) suggests that, together with estrogens, IGF-1, and/or leptin might play a role in the genesis of pubertal gynecomastia.
Persistent pubertal gynecomastia — Pubertal gynecomastia usually resolves spontaneously within six months to two years of onset but, in some instances, it may persist after completion of puberty into adulthood, resulting in persistent pubertal gynecomastia.
Drugs — There are many drugs that have been associated with gynecomastia (table 3). Drugs with the best evidence for an association with gynecomastia are drugs that are known to affect androgen or estrogen concentrations or effects including spironolactone, cimetidine, ketoconazole, recombinant human growth hormone, estrogens, human chorionic gonadotropin (hCG), antiandrogens, gonadotropin-releasing hormone (GnRH) agonists, and 5-alpha-reductase inhibitors [40,41]. The pathophysiologic mechanism for some, such as estrogens or antiandrogens, is quite clear. However, for others such as spironolactone, the mechanisms are multifactorial.
Spironolactone can increase the aromatization of testosterone to E2, decrease the testosterone production rate by the testes, and displace testosterone from sex hormone-binding globulin (SHBG), thereby increasing its metabolic clearance rate. Spironolactone also acts as an antiandrogen by binding to androgen receptors and displacing or preventing binding of testosterone and dihydrotestosterone to their receptors [29,42].
In a placebo-controlled trial of low-dose spironolactone (25 to 50 mg/day) for heart failure, endocrine side effects (gynecomastia, breast pain, impotence, and decreased libido) were seen in 10 percent compared with 3 percent in the placebo group [43]. Gynecomastia will occur in almost every male who takes a large dose of spironolactone (≥100 mg/day), eg, to treat men with liver failure or hypertension due to aldosterone excess [44].
In contrast, in a study of eplerenone (a selective mineralocorticoid receptor antagonist without antiandrogen effects) in over 6500 patients with heart failure, gynecomastia, impotence, or breast pain occurred with equal frequency in the eplerenone and placebo groups (1.0 versus 1.1 percent) [45]. A large meta-analysis confirmed these findings [46]. (See "Secondary pharmacologic therapy in heart failure with reduced ejection fraction (HFrEF) in adults", section on 'Mineralocorticoid receptor antagonist'.)
A large epidemiological study has suggested that statin use might be associated with increased risk of gynecomastia. This case-control study adjusted for a number of factors that are associated with gynecomastia and demonstrated an increased relative risk (20 to 40 percent) of gynecomastia with current, recent, or past use of a statin [47].
For many of the drugs listed in the table, a clear-cut relationship between the drug ingestion and gynecomastia has not been established (table 3). For most drugs, the presumed relationship has been based upon epidemiologic studies or challenge-rechallenge studies in small numbers of individual patients [40,42,48].
Drugs within the same class do not cause gynecomastia to the same extent. Among the calcium channel blockers, nifedipine has the highest frequency of gynecomastia and diltiazem the lowest [42,49]. Thus, in an older man who is at increased risk of gynecomastia simply on the basis of age, diltiazem would be preferable to nifedipine.
Another example is the use of H2-receptor or proton-pump blockers; the incidence of gynecomastia is highest with cimetidine and lowest with omeprazole [50]. Thus, omeprazole would be a better choice in an older individual with other risk factors for developing gynecomastia.
Treatment of HIV infection — The breast enlargement that is seen in men with human immunodeficiency virus (HIV) receiving highly active antiretroviral therapy (HAART) is usually due to fat tissue (lipomastia or pseudogynecomastia) as part of a fat redistribution syndrome (lipodystrophy) [51]. However, cases of true gynecomastia have also been described, thought to be due to coexisting hypogonadism or possible estrogen-like effects of some drugs, in particular, efavirenz [52]. (See "Epidemiology, clinical manifestations, and diagnosis of HIV-associated lipodystrophy" and "Treatment of HIV-associated lipodystrophy".)
Hormone therapy for prostate cancer — Gynecomastia is common in men with prostate cancer undergoing androgen deprivation therapy, in particular with bicalutamide. The prevalence is as high as 75 percent when antiandrogen monotherapy is used but is only approximately 15 percent in men treated with total androgen blockade (combined GnRH agonist with an antiandrogen). This difference might be due to higher doses of antiandrogen plus persistent normal to elevated endogenous production of estrogen with antiandrogen therapy. When antiandrogens are used as monotherapy, much higher doses are used, eg, bicalutamide 150 mg/day versus 50 mg/day if combined with a GnRH agonist. (See "Side effects of androgen deprivation therapy", section on 'Gynecomastia'.)
Herbal products — Tea tree oil and lavender oil, plant-derived oils that are available as over-the-counter skin care products (lotions, soaps, and shampoos), have been associated with gynecomastia. Multiple prepubertal boys have been reported to develop gynecomastia after repeated use of skin products containing the oils [53]. In vitro studies demonstrated weak estrogenic and antiandrogenic properties of both oils, and the gynecomastia resolved when the skin products were discontinued. Other environmental substances with estrogenic or antiandrogenic properties have also been reported to cause gynecomastia [54-56]. Soy protein formulas, which contain high concentrations of phytoestrogens, were not associated with gynecomastia in one study in children [57].
Idiopathic — Gynecomastia in adults is usually multifactorial. There tends to be a gradual decrease in testosterone production in older men and an increase in SHBG levels, resulting in a fall in the total and free testosterone concentration with a reciprocal increase in the luteinizing hormone (LH) level that results in increased aromatization of testosterone to estradiol [27,58]. In addition, aging is associated with increased body fat relative to the lean body mass. Adipose tissue is a site of extraglandular aromatization of testosterone to E2 and of androstenedione to E1. These two factors probably account for most patients who have "idiopathic" gynecomastia. Older men are also more likely to take medications associated with gynecomastia than are younger men.
Cirrhosis — The prevalence of gynecomastia in cirrhotic patients is as high as 67 percent; however, this may not be significantly different from noncirrhotic, age-matched control patients [26,59]. Cirrhosis is accompanied by several changes that probably explain the development of gynecomastia, including an increased production rate of androstenedione from the adrenals, enhanced aromatization of androstenedione to E1, and increased conversion of E1 to E2 [60]. Additionally, many patients receive high doses of spironolactone, which can contribute to the pathogenesis of gynecomastia in this population. (See "Cirrhosis in adults: Etiologies, clinical manifestations, and diagnosis", section on 'Chest findings'.)
Starvation and refeeding — Several studies were carried out on American prisoners of war who were freed at the end of World War II. Approximately 10 percent had developed gynecomastia during starvation, while between 5 and 50 percent noted breast tenderness, pain, and enlargement within two to three months of refeeding after release [61]. Prior to refeeding, approximately 80 percent reported erectile dysfunction, 85 percent had decreased libido, and 73 percent showed testicular atrophy [62]. (See "Causes of secondary hypogonadism in males".)
During starvation, both gonadotropin and testosterone levels were probably reduced, while estrogen production was probably normal due to normal estrogen production from adrenal precursors. These changes will promote the development of gynecomastia. During refeeding, gonadotropins rise, resulting in both an increase in testosterone secretion and a marked elevation in E2 product (due to LH-induced increases in aromatization of testosterone) that mimics normal puberty [62]. Thus, patients who develop refeeding gynecomastia may be said to have undergone a "second puberty." (See "Normal puberty", section on 'Boys'.)
Male hypogonadism — Primary hypogonadism can be due to a congenital abnormality, such as Klinefelter syndrome or an enzymatic defect in the testosterone biosynthetic pathway, or to testicular trauma, infection, infiltrative disorders, vascular insufficiency, or aging (see "Causes of primary hypogonadism in males"). The associated reduction in testosterone production leads to a decrease in the serum testosterone concentration and a compensatory rise in LH release. The excess LH results in enhanced Leydig cell stimulation with inhibition of the 17,20-lyase and 17-hydroxylase activities and increased aromatization of testosterone to E2; the net effect is an increase in E2 relative to testosterone secretion [63].
Secondary hypogonadism due to a hypothalamic or pituitary abnormality is less commonly associated with gynecomastia. In these patients, the production of LH is deficient, resulting in a low testosterone production rate and low E2 production from the testes. However, the adrenal cortex continues to produce estrogen precursors that are aromatized in extraglandular tissue; the result is an increased estrogen-to-androgen ratio.
Men with hyperprolactinemia may develop gynecomastia due to prolactin's effect on reducing the secretion of gonadotropins, leading to secondary hypogonadism. Prolactin itself will stimulate milk production in breast tissue that has been primed by estrogen and progesterone but does not directly cause gynecomastia.
Testicular neoplasms — Germ cell tumors account for approximately 95 percent of testicular neoplasms; between 7 and 11 percent of affected patients have gynecomastia determined by physical examination and 23.4 percent by computed tomography (CT) imaging criteria at the time of presentation [64]. The gynecomastia is associated with secretion of hCG by foci of choriocarcinoma or trophoblastic cells in germ cell tumors (table 3). (See "Anatomy and pathology of testicular tumors".)
The high levels of hCG lead to Leydig cell dysfunction through inhibition of the cytochrome P450c17 enzyme, which mediates the 17,20-lyase and 17-hydroxylase activities in the testes [63]. hCG also stimulates interstitial (Leydig) cell aromatase activity, which converts androgen precursors to E1 and E2. The net effect is a relative increase in E2 to testosterone production.
Gynecomastia is a poor prognostic sign if present at the time of diagnosis of the tumor [64], although this has been disputed [65]. It also occurs in approximately 15 percent of patients after successful treatment with surgery, chemotherapy, or radiation therapy; post-therapy gynecomastia does not affect predicted survival [66]. This form of gynecomastia results from hypogonadism secondary to the chemotherapy or radiation; hCG is not found in the serum. It often spontaneously resolves within one year [66]. (See "Epidemiology of and risk factors for testicular germ cell tumors".)
Gynecomastia is also found in 20 to 30 percent of patients with the less common (2 percent of all testicular tumors) Leydig cell tumors of the testes [67,68]. These tumors are found in 6- to 10-year-old boys who present with precocious puberty and in 26- to 35-year-old men who present with a testicular mass, gynecomastia, erectile dysfunction, and loss of libido. Approximately 10 percent of these tumors are malignant. In boys, Leydig cell tumors may secrete testosterone and/or E2, but they usually secrete relatively increased quantities of E2. They also aromatize androgen precursors to estrogens [69,70]. In adults, testosterone production is generally decreased because the increased E2 levels inhibit gonadotropin secretion, which in turn leads to secondary hypogonadism. (See "Anatomy and pathology of testicular tumors".)
Large cell calcifying Sertoli cell (sex-cord) tumors of the testes are associated with gynecomastia and feminization through excessive aromatase activity, converting androstenedione to E1 and testosterone to E2. These tumors may occur sporadically or as manifestations of two autosomal dominant disorders: Peutz-Jeghers syndrome and the Carney complex. (See "Testicular sex cord stromal tumors", section on 'Sertoli cell tumors'.)
Hyperthyroidism — Gynecomastia has been reported in as many as 25 to 40 percent of men with hyperthyroidism due to Graves' disease, although one study suggests that the prevalence is less than 10 percent [71-74]. Serum LH levels are often elevated, contributing to increased E2 relative to testosterone production by Leydig cells [75,76]. There is also enhanced aromatization of testosterone to E2 and of androstenedione to E1 in extraglandular tissues [77]. This results in increased concentration of SHBG. Free testosterone levels are normal or low, while free E2 levels are elevated. Thus, gynecomastia results from the combination of decreased free androgen levels combined with the overproduction of estrogens. (See "Overview of the clinical manifestations of hyperthyroidism in adults", section on 'Genitourinary'.)
Chronic kidney disease — Gynecomastia occurs in approximately 50 percent of patients treated with maintenance hemodialysis [78]. The primary cause of the gynecomastia appears to be Leydig cell dysfunction. Serum testosterone levels are low, and gonadotropins are appropriately elevated; the metabolic clearance of LH is also reduced [79]. Gynecomastia may occur following renal transplantation as gonadal function improves ("refeeding gynecomastia") and/or the use of transplantation medications such as cyclosporine.
Other rare causes
●Feminizing adrenal tumors – These are rare tumors that are typically large at the time of presentation and are malignant in approximately 75 percent of cases, with a median survival of 1.5 years. In a series of 52 patients, 98 percent had gynecomastia, 58 percent had a palpable tumor, and approximately 50 percent had testicular atrophy [80]. Serum levels of dehydroepiandrosterone sulfate, 17-hydroxyprogesterone, and E2 are increased, while total and free testosterone levels are reduced. Urinary 17-ketosteroid excretion is generally markedly elevated. Gonadotropin levels are usually normal or low. The combination of increased secretion of estrogens by the tumor and increased peripheral aromatization of adrenal androgens to estrogens accounts for the gynecomastia [81]. (See "Clinical presentation and evaluation of adrenocortical tumors", section on 'Androgen and estrogen-secreting tumors'.)
●Ectopic hCG – Increased serum levels of immunoreactive hCG are found in approximately 18 percent of patients with a wide variety of nontrophoblastic neoplasms [82]. The levels of hCG are generally only modestly raised, and most patients do not exhibit clinical evidence of excess hCG production, in part because the majority of patients have production of the biologically inactive free beta subunit of hCG rather than the biologically active intact molecule. There are, however, a few exceptions:
•Precocious puberty can occur in boys with hCG-secreting hepatoblastomas [82].
•In adults, large cell carcinoma of the lung, gastric carcinoma, renal cell carcinoma, and, occasionally, hepatoma have been associated with gynecomastia and marked elevations of serum hCG.
The pathogenesis of the gynecomastia is similar to that found with hCG-secreting germ cell neoplasms of the testes. (See "Clinical manifestations, diagnosis, and staging of testicular germ cell tumors", section on 'Serum tumor markers'.)
●Disorders of sex development – Individuals with a disorder of sex development born with both testicular and ovarian tissue may develop gynecomastia from excessive estrogen secretion by the ovarian component [83]. In addition, the increased estrogen production can suppress intratesticular P450c17 activity, as well as LH secretion, thereby reducing testosterone production.
The androgen insensitivity syndromes are a group of disorders due to defects in or absence of the intracellular androgen receptor in androgen target tissues [84,85]. The clinical manifestations are variable, but breast development is seen. This disorder is reviewed in detail separately. (See "Pathogenesis and clinical features of disorders of androgen action".)
●Familial prepubertal gynecomastia – Familial prepubertal gynecomastia is a rare disorder of increased aromatase activity resulting in severe estrogen excess. The disorder appears to be due to heterozygous inversions or polymorphisms of the p450 aromatase gene (CYP19) [22,86-90]. The mode of inheritance appears to be autosomal dominant [22,88-90].
The initial description was of an eight-year-old boy who had accelerated growth and bone maturation and severe feminization with gynecomastia due to a 50-fold increase in extraglandular conversion of plasma androstenedione to E1 [86]. This child's heterosexual precocity was felt to be due to a failure of fetal aromatase activities to regress following birth.
It is possible that some patients with the diagnosis of "idiopathic" gynecomastia actually represent excessive extraglandular aromatase activity [70].
Aromatase inhibitors, which have had limited success in the treatment of other causes of gynecomastia, may be effective in this disorder [22].
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SUMMARY
●Gynecomastia is defined histologically as a benign proliferation of the glandular tissue of the male breast and clinically by the presence of a rubbery or firm mass extending concentrically from the nipple(s) (figure 1). Fat deposition without glandular proliferation is termed pseudogynecomastia (lipomastia; often seen in obese men). (See 'Definitions' above.)
●Gynecomastia is common in infancy and adolescence. It is estimated that between 60 to 90 percent of infants have transient gynecomastia due to the high estrogenic milieu of pregnancy. The second peak of occurrence is during puberty, affecting approximately one- to two-thirds of boys. Spontaneous regression of breast tissue occurs in most cases. (See "Gynecomastia in children and adolescents".)
●The basic pathophysiology of gynecomastia is an imbalance in androgen-to-estrogen concentrations or effect due to decreased androgen production, increased estrogen production, antiandrogen, or estrogenic drugs or compounds. (See 'Pathophysiology' above.)
●Asymptomatic gynecomastia that incidentally found on examination is very common and likely due to multifactorial causes. (See 'Pathophysiology' above.)
●In adult patients seeking help for gynecomastia, current estimates suggest the following etiologies (table 2) (see 'Epidemiology' above and 'Causes of gynecomastia' above):
•No detectable abnormality – 25 percent
•Persistent pubertal gynecomastia – 25 percent
•Drugs – 10 to 25 percent (table 3)
•Cirrhosis or malnutrition – 8 percent
•Male hypogonadism – 10 percent; (primary hypogonadism [8 percent], secondary hypogonadism [2 percent])
•Testicular tumors – 3 percent
•Untreated hyperthyroidism – 1.5 percent
•Chronic kidney disease – 1 percent
